Rhinology, 46, 144-150, 2008
*Received for publication: October 28, 2008; accepted: February 7, 2008
Sleep apnoea syndrome (SAS) is a growing problem in most
well-developed countries. In a middle age population SAS is
defined as five or more episodes of apnoea or hypopnoea per
hour of sleep
each apnoea or hypopnoea incident must be at least ten sec-
onds long. According to the most often cited study, SAS is
present in 4% of male and 2% of the female population(2).
Clinically, SAS is characterized by recurring apnoeas and
hypopnoeas during sleep, leading to blood desaturation, sleep
fragmentation and many cardio-vascular complications
Nose obstruction, caused by local nasal inflammation has gen-
(1). To fulfil the internationally accepted criteria,
erally been accepted as one of SAS initializing factors
till now, CPAP treatment has been considered as the gold
standard in SAS treatment in patients who do not complain of
nasal obstruction and do not have evidence of anatomical
upper airway obstruction. Clinical data show, that CPAP treat-
ment is not well tolerated by all patients and it is difficult to
predict which patients will not accept this kind of treatment.
Although some studies tried to evaluate the impact of
decreased nasal patency on SAS incidence, as well as on the
effectiveness of CPAP treatment, the exact pathophysiological
mechanism in patients without nasal symptoms has not been
Background: Nasal CPAP has been proven to be an efficient method of treating SAS patients
without facial dysmorphism. However, it still remains a matter of debate why it is not univer-
sally well tolerated.
The aim of the study was to evaluate the influence of initial CPAP treatment on nasal function
in SAS patients.
Patients and methods: Forty-two patients were consecutively included in a prospective clinical
study and divided into the three following groups:
1)SAS subjects (26 patients qualifying for CPAP treatment),
2) First control group (C1) (9 patients with mild or moderate SAS, not willing to be treated
with CPAP, AHI >5 [n/h]),
3) Second control group (C2) (7 healthy subjects, AHI ≤ 5).
Nasal patency was measured by active anterior rhinomanometry (AAR) at recruitment and
after a three-day CPAP treatment. After each AAR nasal lavage was obtained from both nos-
trils. Total inflammatory cell count (TCC) in each nasal lavage was then calculated in a
Results: Initial CPAP treatment caused a statistically significant rise of TCC in nasal lavage of
SAS patients, when compared with initial values [n*105/ml] (pre: 1,30, post: 1,92, p = 0,009).
No significant differences (p > 0,05) were found both in initial TCC and nasal patency values
among the three studied groups.
Conclusions: SAS subjects present an unchanged nasal patency when compared to control sub-
jects. Initial CPAP therapy might be responsible for evoking local nasal inflammation.
Key words: SAS, CPAP, rhinomanometry, nasal lavage
Short-term CPAP treatment induces a mild
increase in inflammatory cells in patients with
sleep apnoea syndrome*
Szymon Skoczynski, Mariola Ograbek-Król, Maciej Tazbirek,
Aleksandra Semik-Orzech, Wladyslaw Pierzchala
Department of Pulmonology, Medical University of Silesia, Katowice, Poland
Footnote: Abbreviations: AHI - apnoea hypopnoea index (number of apnoeas and hypopnoeas during one hour of sleep), BMI - body mass index,
CPAP - continuous positive airway pressure, RNT Bex - nasal expiratory resistance in both nostrils modo Broms, RNT Bin - nasal inspiratory resis-
tance in both nostrils modo Broms, RNT Sex - standard nasal expiratory resistance in both nostrils, RNT Sin - standard nasal inspiratory resistance in
both nostrils, SAS - sleep apnoea syndrome, TCC - total cell count (in 1 ml of nasal lavage).
80831_Skoczynski:80831_Skoczynski 14-05-2008 09:42 Pagina 144
Nasal inflammation and SAS
in SAS and nose function diagnosis, different measuring tools
are used, some of which are still not well-standardized: anteri-
or, posterior or acoustic nasal rhinomanometry, rhinoscopy or
cephalometric measurements. On the other hand, some other
methods useful in the diagnosis of these disorders, like com-
puted tomography, are expensive and include radiation expo-
sure. Nasal patency, its disturbances and main mechanisms of
impairment are important in predicting patient’s future compli-
ance with CPAP therapy. There is evidence of local inflamma-
tion existence in nares of SAS patients(5). The authors showed
that the above-mentioned patients have increased local
neuthrophilia, as well as elevated markers of systemic inflam-
mation (increased plasma levels of CRP, IL-6, and IL-18
On the other hand, there is also evidence that a 4-week
intranasal fluticason therapy significantly lowers AHI in some
patients with rhinitis and SAS
inhibition of local inflammation in those patients might
improve the parameters of nose function. Some epidemiologi-
cal studies show a correlation between the degree of nasal
patency and nostril swelling caused by snoring(8)or the degree
of nasal patency and snoring index in patient’s medical history
(9). Attempts to correlate the degree of nasal obstruction and
sleep disordered breathing were less successful
cited articles nasal patency was measured in a sitting position
(9), while there is strong evidence that the supine position pre-
disposes to its obstruction, by lowering nasal volume
is the reason why we decided to use rhinomanometry in the
supine position. There is evidence of elevated nasal resistance
in SAS patients, although the direct pathomechanism of this
phenomenon has not been established yet
proven that, treating nasal obstruction might reduce obstruc-
tive sleep apnoea severity by decreasing mouth breathing dur-
in subjects being exposed to dry cold air, or other irritating fac-
tors. In recent publications evidence that CPAP without
humidifier does not impair cilary function and mucosal epithe-
lium transport has been shown, however, the small number of
patients enrolled (n=8) makes this result questionable
Published articles tend to indicate different mechanisms of
nasal obstruction in SAS patients like: local inflammation or
swelling, caused by accelerated nasal blood flux
data have also been published about the dominant inflamma-
tion type identified on nasal examination
some evidence that nasal mucosa inflammatory changes occur
with advancing age, leading to worsening of SAS symptoms
and difficulty tolerating CPAP, when used without humidifica-
tion(17,18). On the basis of these data it is difficult to analyze the
precise mechanisms of increased nasal resistance in SAS
patients. It is hard to decide whether SAS is evoked by elevat-
ed nasal resistance or also by nasal obstruction, as other SAS
symptoms influence each other causing symptom worsening.
(4). It is probably caused by the fact, that both,
(7). This could be evidence, that
(8,9). In most
(5,11). It has been
(12). It has also been proven that nasal resistance rises
(15,16). There is also
The aim of our study was to asses the impact of a few-day
CPAP therapy on nasal patency and the number of inflamma-
tory cells in nasal lavage of SAS patients. We compared the
SAS group treated with CPAP to healthy subjects and to
patients with mild SAS who did not accept to be treated by
CPAP. The question was if there were any differences between
SAS patients treated with CPAP and the two control groups, as
far as nose function parameters and nasal cellularity were con-
cerned. We hypothesized, that initial CPAP therapy in some of
the patients might induce local nasal inflammation, explaining
subsequent lack of compliance.
MATERIAL AND METHODS
A total of 59 patients from the Pulmonary Department of the
Medical University of Silesia, were prescreened for the study.
Of these, 42 patients (age between 18 and 65) fulfilled all entry
criteria and were eligible for randomization into one of the
three following groups:
1. Group of 26 SAS subjects (8% female, 92% male, aged 27 to
55 years, mean age 50,2); in which SAS was diagnosed on
the basis of AHI value of > 5 [n/h] (mean AHI: 35,8 ± 18,4)
and the concurrent clinical symptoms of SAS such as: exces-
sive day time sleepiness, disrupted sleep, night choking,
apnoeas during sleep witnessed by bed partner.
2. Control group I (56% female, 44% male, aged 38 to 65 years,
mean age 52,0) – including 9 subjects diagnosed with SAS
(AHI value of > 5 [n/h]); (mean AHI: 12,0 (6,0 - 22,2) who
refused CPAP treatment. All nine subjects gave no consent
for CPAP treatment, either because of relatively little intensi-
ty of clinical symptoms of SAS, or aversion to constant CPAP
usage. All of them were thoroughly informed about the possi-
ble consequences of refusing such treatment; the importance
of body mass reduction was highlighted and/or laryngological
examination in order to consider the usefulness of potential
surgical treatment. To all nine subjects it was also suggested
to repeat polisomnography after 6-12 months.
3. Control group II (29% female, 71% male, aged 26 to 54 years,
mean age 50,0) – including 7 healthy controls, in which SAS
occurrence has been excluded (AHI value of ≤ 5 [n/h] (mean
AHI: 3,0 (0,0 - 5,0); no clinical symptoms of SAS).
The exclusion criteria were as follows: 1) age below 18 and
over 65, 2) smoking history during 6 months before entering
the study, 3) history of upper airway infection for 4 weeks prior
to the preliminary visit and in course of the study, 4) anatomi-
cal anomalies (such as deviated nasal septum) or previous
nasal or sinus surgery, that made it impossible to carry out
AAR, 5) receiving any topical and systemic medication that
might affect nasal patency or local nasal mucosa inflammation
(systemic or topical glucocorticosteroids, histamine-receptor
antagonists, cromoglycate, ketotifen, mast cell stabilizing
drugs and topical decongestants) for 4 weeks prior to the pre-
liminary visit and in course of the study.
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Skoczynski et al.
The study complied with the principles of the Declaration of
Helsinki and its protocol was approved by the Bioethical
Committee of the Silesian Medical University. All patients
gave their written informed consent for the investigation.
During the preliminary visit, complete medical history was
taken and a clinical examination was performed. All subjects
were also asked to complete both the questionnaire for evalu-
ating the probability of SAS occurrence and the Epworth scale.
All subjects were prescreened with a polysomnographic screen-
ing device (STARDUST - Respironiks), performed according
to the standard protocol
patients with AHI < 5 were asked to undergo full night
polysomnography. All subjects checked thus again had, as pre-
viously, AHI < 5.
On the basis of their history, clinical examination and the
results of multi channel sleep screening device all subjects
were further randomized into one of the three studied groups.
The following diagnostic procedures were then performed:
In the group of SAS subjects – active anterior rhinomanometry
and nasal lavage were performed twice: at baseline and after a
three-day CPAP treatment. In both control groups, active ante-
rior rhinomanometry and nasal lavage were performed only
during the preliminary visit.
(19). To avoid the introduction of bias,
Before starting the procedure, subjects were acclimatized and
kept lying flat on their backs for 15 min. AAR was performed,
according to the recommendations of Committee Report on
Standardization of Rhinomanometry(20)in a lying position. An
active anterior rhinomanometer (Rhinotest MP 500, EVG
Electronic-Vertriebs-GmbH, Germany) with foam rubber nose
adapters and a transparent anaesthetic rubber mask was used.
The flow-pressure curves were plotted on-line on the screen
and the measurement was repeated until a stable curve was
obtained during quiet breathing with the mouth closed. For
each nostril, a rhinomanogram was recorded which related
inspiratory and expiratory nasal airflow to transnasal pressure.
The resistances of the left and right cavity separately were cal-
culated from the flow in the fixed gradient pressure of 75 Pa as
the average of 6 consecutive breaths.
Nasal lavage was performed by the „nasal pool“ technique as
described by Greiff and coworkers
saline were instilled into the left and right nasal cavity for 5
min. and then, by decompression, recovered into the plastic
syringe. The mean proportion of lavage fluid recovered was
67,0% ± 3,2%. Nasal lavage fluid was processed immediately
after being recovered. Lavage sample was shaken vigorously to
break up clumps of mucus and 0,1ml of 0,1% dithiothreitol
(Gibco BRL, Warsaw, Poland) was added. Centrifugation (5
min. at 500g) of saline washings separated cell pellet and super-
natant. The supernatant was discarded and the obtained sedi-
ment was suspended in 1 ml of sterile phosphate buffered
saline (PBS, Sigma). After staining the cells with the Kimura
method, the total number of non-squamous cells was counted
with the use of a Neubauer hemocytometer, allowing determi-
nation of the number of cells in 1 ml of recovered fluid.
(21). Six ml of warm, sterile
The statistical evaluation was performed with a statistical soft-
ware package (Statistica 6.0). Results are expressed as mean
values ± SD or medians and ranges (maximal and minimal val-
ues are in brackets). The Kolmogorov-Smirnov test was used
to test variables for normal distribution. Depending on the dis-
tribution, Student t test, Wilcoxon signed-rank test or Kruskal-
Wallis test were used for inter-group comparisons. Pre-post
Table 1. General characteristics of study subjects.
Subjects with SAS
Control group I
Control group II
Data are expressed as medians and ranges (maximal and minimal values are in brackets).
*p value for inter-group comparisons (Kruskal-Wallis test)
F – females, BMI – body mass index, WHR – waste to hip ratio, AHI –apnoea and hypopnoea index, O2sat- average minimal saturation achieved
during screening polysomnography, CPAP –continuous positive airway pressure, ND – Not Done, NS – Non significant.
80831_Skoczynski:80831_Skoczynski 14-05-2008 09:42 Pagina 146
Nasal inflammation and SAS
treatment differences were evaluated, depending on the distri-
bution, using Student t test or Wilcoxon test. P values of <
0,05 were accepted as statistically significant.
Main baseline characteristics of the included patients are sum-
marized in Table 1. Twenty-six subjects with SAS that under-
went CPAP treatment, 9 SAS subjects that refused CPAP
treatment and 7 healthy controls were enrolled in the study.
All studied groups were comparable in respect to age, BMI and
WHI values. When compared to control groups, at entry, sub-
jects with SAS exhibited significantly higher AHI (p < 0,001;
Kruskal-Wallis test), and average minimal blood saturation val-
ues during night screening (p = 0,026; Kruskal-Wallis test).
On average, effective CPAP pressure values of 9,0 (4,0 - 12,0)
[mbar] were applied in the first group of SAS subjects. The
mean value of AHI achieved after initial CPAP treatment was
within physiological range, averaging 4,83 ± 3,38. This proves
that the applied treatment was highly effective.
No statistically significant differences were found between rhi-
nomanometric parameters at baseline between all groups
(Table 2). In the group of SAS subjects, CPAP treatment did
not induce any significant changes in any of the rhinomano-
metric parameters (Table 3).
No statistically significant differences were found in the total
non-epithelial cell count in nasal lavage between the studied
groups at baseline (p = 0,907; Kruskal-Wallis test) (Figure 1).
In the group of SAS subjects CPAP treatment induced a statis-
tically significant increase of 47% in the number of non-epithe-
lial cells in the nasal lavage, as compared to baseline [n*105/ml
Figure 1. Comparison of initial nasal lavage cellularity in studied
The inter-group comparison of baseline lavage total cell count revealed
no significant differences between the three studied groups (p > 0,05,
Figure 2. Evolution of total non-epithelial cell count in nasal lavage of
SAS subjects after initial CPAP treatment.
Short-term CPAP treatment significantly increased nasal lavage
cellularity of SAS subjects when compared to baseline values (pre-post
comparison, Student t test).
Table 2. Comparison of initial values of rhinomanometric parameters between studied groups.
Rhinomanometric Subjects with SAS
Data are expressed as medians and ranges (maximal and minimal values are in brackets).
*p value for inter-group comparisons (Kruskal-Wallis test), RNT Sex - standard nasal expiratory resistance in both nostrils, RNT Sin - standard nasal
inspiratory resistance in both nostrils RNT Bex - nasal expiratory resistance in both nostrils modo Broms, RNT Bin - nasal inspiratory resistance in
both nostrils modo Broms, NS – Non significant.
Control group I Control group IIp*
80831_Skoczynski:80831_Skoczynski 14-05-2008 09:42 Pagina 147
Skoczynski et al.
of lavage]: (pre-treatment values: 1,30 ± 1,15; post-treatment
values: 1,92 ± 1,51; p = 0,009; Student t test) (Figure 2).
To start our discussion it is necessary to explain the cut-off
point (AHI value of ≤ 5 [n/h] accepted by our team for sleep
apnoea. As mentioned before, we have accepted the diagnostic
criteria by the American Academy of Sleep Medicine Task
other criteria based on different AHI cut-off points (5, 10, 15)
used by different authors to diagnose SAS. The reason for such
discrepancies is the variability in scoring hypopnoea, which also
complicates between-study comparisons. In most cases SAS is
effectively treated with nasal CPAP. CPAP is considered as a
well-accepted method of treatment in SAS patients without
nose obstruction(22). Patients with nasal obstruction or anatom-
ical abnormalities of the facial skeleton should undergo surgical
treatment. SAS patients often complain of nasal symptoms
before and during CPAP. This might be the result of increased
nasal resistance, which predisposes to upper airway obstruction
and consequently to snoring
CPAP treatment might be responsible for symptoms such as
running nose and sneezing
tent with the above. However, as nasal patency of SAS subjects
did not change during our study, the increased cell count after
CPAP treatment could have been an effect of pre-existing dis-
ease. To minimize this possibility we excluded subjects with
history of rhinorhea or nasal obstruction. We have also exclud-
ed patients treated with systemic and/or local drugs, which
might potentially interfere with nasal function and influence
CPAP usage compliance, such as systemic or topical glucocorti-
costeroids, histamine-receptor antagonists, cromoglycate, keto-
tifen, mast cell stabilizing drugs and topical decongestants.
(1). However, it should be stressed, that there are also
(23). There is also evidence that
(24). Our findings are partly consis-
after 6 months of CPAP usage. In our research we decided to
assess the nasal function after three days of CPAP therapy. We
were fully aware that this relatively short observation time
might be considered as one of the study limitations. However,
we wanted to avoid possible influence of seasonal factors (e.g.
pollens, upper respiratory tract infections) on nasal patency and
potential local inflammation. However, this relatively short
observation period of three days has not been completely free
from other interfering factors, such as an increased risk of
upper airway nosocomial infection. In contrast to some other
paranasal X-ray, CT and anterior rhinoscopy, our study aimed
to assess nasal function using AAR. CPAP with humidifiers
were not used in our study, as it has been proven that humidi-
fiers significantly reduce upper airway side effects and lead to
better CPAP compliance
polysomnography - the golden standard in SAS diagnosis - in
our study we have used multi channel sleep studying devices,
as it has been proven that they can accurately make a diagnosis
of SAS when daytime symptoms coexist
as a potential source of methodological bias, we have asked
patients without SAS (AHI ≤ 5 [n/h]) - as confirmed by multi
channel screening device (STARDUST-by Respironics) - to
additionally undergo a whole night polysomnography test
(Alice 4, Respironics). In all of those cases (50% of subjects
enrolled to control group 2) the diagnosis did not change.
Increased nasal patency is not the only factor, which influences
acceptance of CPAP therapy
compliance are: discomfort caused by the face mask, limitation
in movements during sleep, claustrophobia, eye irritation by air
leakage, allergy to the mask, effect on bed partners, relatively
mild day time symptoms and many others that were not ana-
lyzed in the present study.
(24)compared different nasal function parameters
(25)in which the authors used mainly
(18). Instead of completing full night
(19). To minimize this
(26). Other factors affecting CPAP
According to previous studies low AHI values may predict
with high accuracy that CPAP will not be tolerated. We
assume that this was a reason why some of the patients with
mild to moderate SAS did not want to use CPAP. Patients
enrolled in this group were discharged from the Pulmonary
Department with the recommendation for laryngological treat-
ment and active weight reduction. They were also requested to
undergo follow up polysomnography after 6 to 12 months. In
contrast to Sugiara et al.(26)acceptance of CPAP therapy in our
patients correlated positively with AHI but not with nasal
patency. In our study nasal patency and cell markers of nose
inflammation were evaluated simultaneously. That is why our
study, as a multi factor nasal control research, provides wider
view on the analyzed problem than most of the studies previ-
The presence of a systemic inflammatory state in SAS patients
is well proven
oxidative stress accelerates systemic inflammation in this pop-
(27). Scientists and clinicians agree that recurrent
Table 3. Evolution of rhinomanometric parameters induced by initial
CPAP treatment in group of SAS subjects.
Data are expressed as medians and ranges (maximal and minimal
values are in brackets).
*P value for pre-post comparisons (Student t test), CPAP - continuous
positive airway pressure, RNT Sex - standard nasal expiratory
resistance in both nostrils, RNT Sin - standard nasal inspiratory
resistance in both nostrils RNT Bex - nasal expiratory resistance in
both nostrils modo Broms, RNT Bin - nasal inspiratory resistance in
both nostrils modo Broms, NS – Non significant.
80831_Skoczynski:80831_Skoczynski 14-05-2008 09:42 Pagina 148
Nasal inflammation and SAS
ulation and leads to a metabolic syndrome characterized by
atherosclerosis and shorter life expectancy. Cardio-vascular
complications are one of the most frequent causes of death in
A systemic inflammatory state is not the only manifestation of
inflammation in the SAS population. Several authors seem to
propose different mechanisms of cell and cytokine infiltration
of the upper airways. The influence of an increased oxidative
airway stress has been proven by increased levels of IL-6 and
8-Isoprostane in exhaled breath condensate in SAS subjects
(28). SAS children have a higher neutrophil concentration
well as other inflammatory mediators such as leukotrienes and
prostaglandins(30)collected from the upper airways. In contrast
to systemic findings, the influence of CPAP treatment on local
nasal inflammation has not been established yet. There is evi-
dence that in some cases nasal CPAP may induce airway
intranasal inflammation in SAS patients, which would explain
the existence of upper airway obstruction in non-smoking SAS
patients(4). This is caused by an increased number of polymor-
phonuclear leukocytes and a high bradykinin concentration(4).
(31). There is also some data on local
The significant changes found in lavage cellularity after initial
CPAP treatment in SAS subjects open wider diagnostic and
treatment possibilities in this disease. Further research including
a longitudinal analysis of nasal lavage differential cell count and
other inflammatory markers present in nasal secretions and
blood, could help to elucidate the exact pathomechanisms
responsible for poor CPAP compliance. Assessment of domi-
nant inflammatory cell types in SAS patients would lead to diag-
nosing the exact pattern of inflammation and allow cause-specif-
ic treatment. Finally, some authors speculate that CPAP treat-
ment reduces local and systemic inflammation
suggest a role for a pharmacological method in SAS co-treat-
ment. According to our findings, nasal CPAP treatment initially
leads to local nasal inflammation. This fact requires further
investigation and assessment during longer observation periods.
(32). This may
Initial CPAP treatment in SAS patients induces local inflam-
mation documented by increased nasal lavage cellularity with-
out concurrent nasal obstruction.
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Szymon Skoczynski MD
Department of Pulmonology
Medical University of Silesia
40-752 Katowice, ul. Medyków 14
Tel: +48-50-251 9026
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